Roy A. Wise, Ph.D., F.R.S.C.

@article{Wise:2009aa,

title = {Roles for nigrostriatal--not just mesocorticolimbic--dopamine in reward and addiction.},

author = {Roy A Wise},

url = {https://www.ncbi.nlm.nih.gov/pubmed/19758714},

doi = {10.1016/j.tins.2009.06.004},

issn = {1878-108X (Electronic); 0166-2236 (Linking)},

year  = {2009},

date = {2009-10-01},

journal = {Trends Neurosci},

volume = {32},

number = {10},

pages = {517--524},

address = {Behavioral Neuroscience Branch, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, USA. rwise@intra.nida.nih.gov},

abstract = {Forebrain dopamine circuitry has traditionally been studied by two largely independent specialist groups: students of Parkinson's disease who study the nigrostriatal dopamine system that originates in the substantia nigra (SN), and students of motivation and addiction who study the role of the mesolimbic and mesocortical dopamine systems that originate in the ventral tegmental area (VTA). The anatomical evidence for independent nigrostriatal and mesolimbic dopamine systems has, however, long been obsolete. There is now compelling evidence that both nominal "systems" participate in reward function and addiction. Electrical stimulation of both SN and VTA is rewarding, blockade of glutamatergic or cholinergic input to either SN or VTA attenuates the habit-forming effects of intravenous cocaine, and dopamine in both nigrostriatal and mesocorticolimbic terminal fields participates in the defining property of rewarding events: the reinforcement of memory consolidation. Thus, the similarities between nigrostriatal and mesolimbic dopamine systems can be as important as their differences.},

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pubstate = {published},

tppubtype = {article}

}

@article{You:2008aa,

title = {Acetylcholine release in the mesocorticolimbic dopamine system during cocaine seeking: conditioned and unconditioned contributions to reward and motivation.},

author = {Zhi-Bing You and Bin Wang and Dawnya Zitzman and Roy A Wise},

url = {https://www.ncbi.nlm.nih.gov/pubmed/18768696},

doi = {10.1523/JNEUROSCI.0694-08.2008},

issn = {1529-2401 (Electronic); 0270-6474 (Linking)},

year  = {2008},

date = {2008-09-03},

journal = {J Neurosci},

volume = {28},

number = {36},

pages = {9021--9029},

address = {Behavioral Neuroscience Branch, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Department of Health and Human Services, Baltimore, Maryland 21224, USA. zyou@intra.nida.nih.gov},

abstract = {Microdialysis was used to assess the contribution to cocaine seeking of cholinergic input to the mesocorticolimbic dopamine system in ventral tegmental area (VTA). VTA acetylcholine (ACh) was elevated in animals lever pressing for intravenous cocaine and in cocaine-experienced and cocaine-naive animals passively receiving similar "yoked" injections. In cocaine-trained animals, the elevations comprised an initial (first hour) peak to approximately 160% of baseline and a subsequent plateau of 140% of baseline for the rest of the cocaine intake period. In cocaine-naive animals, yoked cocaine injections raised ACh levels to the 140% plateau but did not cause the initial 160% peak. In cocaine-trained animals that received unexpected saline (extinction conditions) rather than the expected cocaine, the initial peak was seen but the subsequent plateau was absent. VTA ACh levels played a causal role and were not just a correlate of cocaine seeking. Blocking muscarinic input to the VTA increased cocaine intake; the increase in intake offset the decrease in cholinergic input, resulting in the same VTA dopamine levels as were seen in the absence of the ACh antagonists. Increased VTA ACh levels (resulting from 10 microM VTA neostigmine infusion) increased VTA dopamine levels and reinstated cocaine seeking in cocaine-trained animals that had undergone extinction; these effects were strongly attenuated by local infusion of a muscarinic antagonist and weakly attenuated by a nicotinic antagonist. These findings identify two cholinergic responses to cocaine self-administration, an unconditioned response to cocaine itself and a conditioned response triggered by cocaine-predictive cues, and confirm that these cholinergic responses contribute to the control of cocaine seeking.},

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pubstate = {published},

tppubtype = {article}

}

@article{Geisler:2008aa,

title = {Functional implications of glutamatergic projections to the ventral tegmental area.},

author = {Stefanie Geisler and Roy A Wise},

url = {https://www.ncbi.nlm.nih.gov/pubmed/19145985},

issn = {0334-1763 (Print); 0334-1763 (Linking)},

year  = {2008},

date = {2008-08-31},

journal = {Rev Neurosci},

volume = {19},

number = {4-5},

pages = {227--244},

address = {Behavioral Neuroscience Branch, Department of Health and Human Services, National Institutes of Health, National Institute on Drug Abuse, Intramural Research Program, Baltimore, MD 21224, USA. GeislerS@mail.nih.gov},

abstract = {Glutamatergic afferents of the ventral tegmental area (VTA) play an important role in the functioning of the VTA and are involved in the pathophysiology of drug addiction. It has recently been demonstrated that the VTA is densely innervated by glutamatergic axons and that glutamatergic neurons projecting to the VTA are situated in almost all structures that project there. While the projection from the prefrontal cortex is essentially entirely glutamatergic, subcortical glutamatergic neurons innervating the VTA intermingle with non-glutamatergic, most likely GABAergic and/or peptidergic VTA-projecting neurons. The first part of this review focuses on the origins and putative functional implications of various glutamatergic projections to the VTA. In the second part we consider how different neuropeptides via different mechanisms modulate glutamatergic actions in the VTA. We conclude by developing a model of how the glutamatergic afferents might together contribute to the functions of the VTA.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Wise:2008aa,

title = {Cocaine serves as a peripheral interoceptive conditioned stimulus for central glutamate and dopamine release.},

author = {Roy A Wise and Bin Wang and Zhi-Bing You},

url = {https://www.ncbi.nlm.nih.gov/pubmed/18682722},

doi = {10.1371/journal.pone.0002846},

issn = {1932-6203 (Electronic); 1932-6203 (Linking)},

year  = {2008},

date = {2008-08-06},

journal = {PLoS One},

volume = {3},

number = {8},

pages = {e2846},

address = {Department of Health and Human Services, Behavioral Neuroscience Branch, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland, United States of America. rwise@intra.nida.nih.gov},

abstract = {Intravenous injections of cocaine HCl are habit-forming because, among their many actions, they elevate extracellular dopamine levels in the terminal fields of the mesocorticolimbic dopamine system. This action, thought to be very important for cocaine's strong addiction liability, is believed to have very short latency and is assumed to reflect rapid brain entry and pharmacokinetics of the drug. However, while intravenous cocaine HCl has almost immediate effects on behavior and extracellular dopamine levels, recent evidence suggests that its central pharmacological effects are not evident until 10 or more seconds after IV injection. Thus the immediate effects of a given intravenous cocaine injection on extracellular dopamine concentration and behavior appear to occur before there is sufficient time for cocaine to act centrally as a dopamine uptake inhibitor. To explore the contribution of peripheral effects of cocaine to the early activation of the dopamine system, we used brain microdialysis to measure the effects of cocaine methiodide (MI)--a cocaine analogue that does not cross the blood brain barrier--on glutamate (excitatory) input to the dopamine cells. IP injections of cocaine MI were ineffective in cocaine-naive animals but stimulated ventral tegmental glutamate release in rats previously trained to lever-press for cocaine HCl. This peripherally triggered glutamate input was sufficient to reinstate cocaine-seeking in previously trained animals that had undergone extinction of the habit. These findings offer an explanation for short-latency behavioral responses and immediate dopamine elevations seen following cocaine injections in cocaine-experienced but not cocaine-naive animals.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{You:2007aa,

title = {A role for conditioned ventral tegmental glutamate release in cocaine seeking.},

author = {Zhi-Bing You and Bin Wang and Dawnya Zitzman and Soraya Azari and Roy A Wise},

url = {https://www.ncbi.nlm.nih.gov/pubmed/17898226},

doi = {10.1523/JNEUROSCI.2967-07.2007},

issn = {1529-2401 (Electronic); 0270-6474 (Linking)},

year  = {2007},

date = {2007-09-26},

journal = {J Neurosci},

volume = {27},

number = {39},

pages = {10546--10555},

address = {Behavioral Neuroscience Branch, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland 21224, USA. zyou@intra.nida.nih.gov},

abstract = {Initiation of cocaine self-administration in rats was associated with release of glutamate in the ventral tegmental area (VTA). The glutamate release was transient, despite continued cocaine intake. Similar glutamate release was seen in rats earning, for the first time, unexpected saline rather than expected cocaine. VTA glutamate release was not seen in similarly trained rats earning saline instead of cocaine for the 13th time. VTA glutamate release was also seen in similarly trained rats that received yoked rather than earned cocaine injections on test day. VTA glutamate release was not seen in a group of rats that had never earned cocaine but had received yoked injections during the training period. Glutamate release was also not seen in a group of rats that received yoked injections but had no previous experience with cocaine. VTA GABA levels did not fluctuate during any aspect of cocaine seeking. Blockade of VTA glutamate receptors appeared to attenuate the rewarding effects of intravenous cocaine injections and blocked almost completely the conditioned responding normally seen during extinction trials. These findings indicate that VTA glutamate release is a conditioned response dependent on an associative process and is not a simple consequence of previous cocaine exposure. The findings implicate glutamate as at least one of the sources of VTA signals from reward-associated environmental stimuli.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Wang:2005aa,

title = {Cocaine experience establishes control of midbrain glutamate and dopamine by corticotropin-releasing factor: a role in stress-induced relapse to drug seeking.},

author = {Bin Wang and Yavin Shaham and Dawnya Zitzman and Soraya Azari and Roy A Wise and Zhi-Bing You},

url = {https://www.ncbi.nlm.nih.gov/pubmed/15930388},

doi = {10.1523/JNEUROSCI.0955-05.2005},

issn = {1529-2401 (Electronic); 0270-6474 (Linking)},

year  = {2006},

date = {2006-06-01},

journal = {J Neurosci},

volume = {25},

number = {22},

pages = {5389--5396},

address = {Behavioral Neuroscience Branch, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland 21224, USA.},

abstract = {Footshock stress can reinstate cocaine-seeking behavior through a central action of the stress-associated neurohormone corticotropin-releasing factor (CRF). Here we report (1) that footshock stress releases CRF in the ventral tegmental area (VTA) of the rat brain, (2) that, in cocaine-experienced but not in cocaine-naive rats, this CRF acquires control over local glutamate release, (3) that CRF-induced glutamate release activates the mesocorticolimbic dopamine system, and (4) that, through this circuitry, footshock stress triggers relapse to drug seeking in cocaine-experienced animals. Thus, a long-lasting cocaine-induced neuroadaptation, presumably at the level of glutamate terminals in the VTA, appears to play an important role in stress-induced relapse to drug use. Similar neuroadaptations may be important for the comorbidity between addiction and other stress-related psychiatric disorders.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Wise:2004ab,

title = {Dopamine, learning and motivation.},

author = {Roy A Wise},

url = {https://www.ncbi.nlm.nih.gov/pubmed/15152198},

doi = {10.1038/nrn1406},

issn = {1471-003X (Print); 1471-003X (Linking)},

year  = {2004},

date = {2004-06-05},

journal = {Nat Rev Neurosci},

volume = {5},

number = {6},

pages = {483--494},

address = {Behavioral Neuroscience Branch, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Bethesda, Maryland 20892, USA. rwise@intra.nida.nih.gov},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Wise:2004aa,

title = {Drive, incentive, and reinforcement: the antecedents and consequences of motivation.},

author = {Roy A Wise},

url = {https://www.ncbi.nlm.nih.gov/pubmed/15160641},

issn = {0146-7875 (Print); 0146-7875 (Linking)},

year  = {2004},

date = {2004-01-01},

journal = {Nebr Symp Motiv},

volume = {50},

pages = {159--195},

keywords = {},

pubstate = {published},

tppubtype = {article}

}